Hyperparathyroidism

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Hyperparathyroidism

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Hyperparathyroidism (HPT) results when there is excessive secretion of parathyroid hormone (PTH).[1] PTH is secreted by the four parathyroid glands, located in the neck behind the thyroid gland. It regulates serum calcium and phosphate levels and also plays a part in bone metabolism. High levels of PTH cause serum calcium levels to increase and serum phosphate levels to fall.

70-80% of people are asymptomatic and diagnosis is made after incidental hypercalcaemia is found. In those who are symptomatic, remember: 'bones, stones, abdominal groans, and psychic moans'.

Clinical features are due to:

Excessive calcium resorption from bone:

Osteopenia and osteoporosis, presenting as bone pain and pathological fractures.

Osteitis fibrosa cystica can occur in severe cases. It presents with subperiosteal resorption of the distal phalanges, tapering of the distal clavicles, salt and pepper appearance of the skull, and brown tumours of the long bones.

25-hydroxyvitamin D (25(OH)D) should be measured if PTH raised; there is evidence that HPT is more active when patients are vitamin D-depleted.[2]There is also evidence that raised PTH levels can reduce when low 25(OH)D levels are corrected. See also 'Secondary hyperparathyroidism', below.

Dual-energy X-ray absorptiometry (DEXA) scan can show any skeletal involvement in PHPT.

Pathognomonic X-ray changes include salt and pepper degranulation in the skull and subperiosteal bone resorption in the phalanges in severe cases.

Treatment

Surveillance can be used in patients with mildly elevated calcium levels and close to normal renal and bone status.[3]

All patients should be replete in vitamin D, aiming for a minimum serum level of 25(OH)D >20 ng/dL. 800 to 1000 IU are a useful starting dose.

Such patients may continue for long periods without deterioration in bone mineral density.

However, progression can occur: at 15 years one third of patients will have overt features of HPT, such as kidney stones, worsening hypercalcaemia and reduced bone density.

Monitor for overt signs and symptoms of PHPT. However there is controversy over what constitutes 'asymptomatic', as the symptoms of PHPT can be nonspecific and subtle, such as fatigue, weakness and muscle pains.[4]

There is development of a kidney stone, either clinically or by imaging.

Bone mineral density T score is less than -2.5 (at any site) or there is a significant reduction in bone mass density.

There is a vertebral fracture.

Patient request is also an appropriate indication, especially if follow-up is unlikely.

While there is subtle evidence that patients with PHPT may have cardiovascular dysfunction, there is no evidence that surgery for PHPT affects cardiovascular endpoints .

Minimally invasive parathyroidectomy in combination with pre-operative localisation investigations is increasingly being used. These investigations include ultrasound, MRI, computerised axial tomography and technetium 99m Tc-labelled sestamibi single-photon emission CT. However, they play no part in the diagnosis of PHPT.[4]

Parathyroid surgery should only be performed by highly experienced surgeons .

Intraoperative measurement of PTH may also help to see if the abnormal gland(s) has been removed. The PTH level drops by 50% within 10-15 minutes of the hyper-functioning parathyroid tissue being removed.

Medical treatment

Medical management is used for those who opt against surgery or who do not meet the criteria for surgery.[5]

HRT and raloxifene may be used in postmenopausal women. They have been shown to reduce calcium levels as well as improve bone density.[1] However, because of the risks associated with oestrogen replacement, it should not be used purely to treat PHPT.

Bisphosphonates (particularly alendronate) may be a useful treatment.[1]

Complications after surgery

These include:

Hypocalcaemia - due to 'hungry bone syndrome'. Calcium and phosphorus are rapidly deposited in bone. There is hypoparathyroidism and transient, sometimes severe, hypocalcaemia until the normal glands regain sensitivity. If hypoparathyroidism persists, calcium and vitamin D supplements are required.

The National Institute for Health and Care Excellence (NICE) only recommends the use of cinacalcet for those people with end-stage kidney disease whose SHPT is refractory to other treatment and in whom surgery is not suitable as a treatment.[8]

Trials indicate that early intervention in stages 3 and 4 of CKD can correct PTH levels and could prevent renal bone disease, reduce cardiovascular complications and prolong patient survival.[6]

Parathyroidectomy may be considered in severe cases refractory to medical treatment.

There is a 10% risk of recurrent or persistent disease after parathyroidectomy.

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